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The role of fetal inflammatory response syndrome and fetal anemia in nonpreventable term neonatal encephalopathy

Abstract

Objective:

To evaluate asphyxial patterns in term encephalopathic newborns caused by chorioamnionitis or intrapartum blood loss that resulted in cerebral palsy and allegations of obstetrical professional liability.

Study Design:

As an expert witness, JKM identified term newborns with profound neurologic impairment: 18 born in the presence of chorioamnionitis and 14 with significant anemia.

Result:

In both study groups, profound depression with low 10-min Apgars was associated with early-onset seizures (88%), multiorgan failure (94%) and a partial prolonged injury to the cortex and subcortical white matter (94%). A cord arterial pH>7.00 was noted in 68% and deep gray matter injury involving the basal ganglia and thalamus occurred in only 19% of the newborns studied.

Conclusion:

The cord arterial pH and pCO2 values, early-onset seizures and paucity of isolated deep gray matter injury support that significant injury occurred postnatally despite appropriate resuscitation. This unique pattern may refute allegations of obstetrical mismanagement in the intrapartum period.

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Correspondence to J K Muraskas.

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Muraskas, J., Kelly, A., Nash, M. et al. The role of fetal inflammatory response syndrome and fetal anemia in nonpreventable term neonatal encephalopathy. J Perinatol 36, 362–365 (2016). https://doi.org/10.1038/jp.2015.214

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